A Dissertation On
A CLINICAL ANALYSIS OF 50 CASES OF PATHOLOGICAL MYOPIA
Submitted to
THE TAMILNADU DR. M.G.R MEDICAL UNIVERSITY CHENNAI
With fulfillment of the regulations for the award of the degree of M.S (OPHTHALMOLOGY)
BRANCH-III
REGIONAL INSTITUTE OF OPHTHALMOLOGY GOVT.OPHTHALMIC HOSPITAL
MADRAS MEDICAL COLLEGE CHENNAI
CERTIFICATE
This is to certify that this dissertation entitled A CLINICAL ANALYSIS OF 50 CASES OF PATHOLOGICAL MYOPIA
submitted by Dr.R.UMA MAHESHWARI appearing for Part II M.S
Branch III (OPHTHALMOLOGY) degree examination in February 2007 is a bonafide record of work done by her under my direct audience and supervision in partial fulfillment of regulations of the Tamil Nadu, Dr.M.G.R.Medical University ,CHENNAI,TAMILNADU.I forward this to the Tamil Nadu , Dr.M.G.R.Medical University Chennai, Tamil Nadu, India.
Prof .Dr.K.ASOKAN.M.S.,D.O., Prof.DrV.VELAYUTHAM,M.S.,D.O
Unit Chief ,Retina clinic Director and Supertinentendent Regional Institute of Ophthalmology Regional Institute of Ophthalmology Government Ophthalmic Hospital Government Ophthalmic Hospital, Egmore, Chennai Egmore, Chennai
Prof. Dr. KALAVATHY PONNIRAIVAN, B.Sc, M.D
Dean, Madras Medical College & Government General Hospital,
DECLARATION
I, Dr. Uma Maheshwari solemnly declare that the dissertation
titled “A CLINICAL ANALYSIS OF 50 CASES OF
PATHOLOGICAL MYOPIA” has been prepared by me. This is submitted to The Tamil Nadu Dr. M.G.R. Medical University, Chennai,
in partial fulfilment of the requirement for the award of M.S.,
degree Examination to be held in March 2007.
Place: Chennai
ACKNOWLEDGEMENT
I express my sincere thanks to Dean Dr.KALAVATHY PONNIRAIVAN., B.Sc ,M.D, for granting me permission to conduct this study .
I have great pleasure in thanking prof V.VELAYUTHAM
M.S.,D.O, Director &Superintendent, Regional Institute of Ophthalmology & Government Ophthalmic Hospital,Chennai for having assigned me this topic & for his best inspiration and kind help.
I express my profound gratitude to prof K.ASOKAN., M.S.,
D.O, Chief,Vitreo-Retina clinic of RIO-GOH for his expert guidance & unfailing assistance offered to me during the entire period of work & for the successful accomplishment of this task.
I am very grateful to all my unit assistant professors,
Dr.B.Easwaraj M.S.,D.O., Dr.K.Rajasekar M.S(Ophthal)., and Dr.C.L. Chitra. D.O.,DNB for rendering their valuable advice and help during the study.
I wish to express to express my sincere thanks to all the Professors, Asst. Professors and all my colleagues who have helped me in completing this study.
CONTENTS
S.No TITLE PAGE No. PART –I
1. INTRODUCTION
1
2. HISTORICAL REVIEW
3
3. ANATOMY
5
4. EPIDEMIOLOGY
11
5. OPTICS OF EYE
12
6. CLASSIFICATION OF MYOPIA
14
7. PATHOGENESIS
16
8. CLINICAL EVALUATION
28
9. MANAGEMENT
30
PART-II
1. AIM OF THE STUDY
34
2. MATERIALS &METHODS
PART-III
1. BIBLIOGRAPHY
2. PROFORMA
3. KEY TO MASTER CHART
4. MASTER CHART
5. LIST OF SURGERIES PERFORMED
INTRODUCTION
Eye is the most important sense organ of the human body. The
primary responsibility of the visual function is carried out by retina.
Pathological changes of retina can cause irreversible blindness. Myopia
causes impaired visual acquity among school children as well as in
adults. Retinal degeneration and retinal detachment is also commonly in
myopic patients.
The retina is unique among the complex element of the central
nervous system and the special senses.It may be readily viewed during
life, and it is sufficiently transparent so that alterations within and
adjacent to it may be observed in vivo.
For these and other reasons related to its structure , organization
and function , the retina has been the ever- increasing importance in
Consistence with this growing importance, methods of viewing
the etina have steadily improved during more than a century since the
principal of ophthalmoscopy was presented by Von- Helmhotz. As a
result, current techniques of ophthalmoscopy and biomicroscopy
facilitate clinical examination of the entire retina in detail.
Interpretations of the findings, however , depend on the accurate
and detailed knowledge of retinal topography, anatomical relationships,
common developmental variations and degenerations that commonly
affect the retina.
Eyes with pathologic myopia are an eccentric group in which the
myopia is more likely due to a disease than to a biologic variation.such
eyes show excessive axial length with equatorial scleral expansion
,dehiscences and posterior staphyloma formation.Global expansion can
slowly progress during a persons life time and result in blinding
complications. Pathologically myopic eyes have erros of -6.00 D or
greater,in excess of -40.00 D. With recent technologies like Bscan,
ICG,FFA and OCT we are able to understand and monitor the
underlying pathology and structural alterations in a better manner.
HISTORICAL REVIEW
The word myopia is derived from the Greek word müopia, which means contracting or closing the eyes.
ARISTOTLE- first person who noted the tendency of myopes to blink and write in small script
FRANS CORNELIS DONDERS (1818-1889)- first to analyse the various types of refractive error.
NEWTON (1704)- noted that axial length is the sole determinant of refraction.
PLEMPIUS (1632)- proved that in myopes the axial length is more
SCARDIA (1801) - The first person who anatomically described posterior staphyloma.
VON AMMON (1832)- pointed out that posterior staphyloma was due to distension of the posterior pole.
VON GRAEYE and VON JAEGER (1854) – postulated the association of myopia and posterior staphyloma.
ARLT (1856) – association of myopia with axial elongation.
REHSTEINER (1928) - .noted the peripheral degenerative changes in pathological myopia.
STENSTROM (1946) – Measured the ocular axial length directly by X-rays.
KREMER and Co-workers – high myopes showed the presence of multiple atrophic retinal holes in the posterior pole.
BURTON – refractive error and lattice degeneration on detachment.
MORITA and Coworkers – risk factors associated with retinal detachment
ANATOMY AND TOPOGRAPHY OF RETINA
CENTRAL RETINA
The retina proper is a thin, delicate layer of nervous tissue that
has a surface area of about 266 mmsq.The major landmarks of the retina
are the optic disc, the retinal blood vessels, the area centralis with
fovea and foveola, the peripheral retina (which includes the equator) and the ora serrata.The retina is thickest near the optic disc , where it measures 0.56 mm,becomes thinner towards the periphery.
THE OPTIC DISC
The optic nerve head, the collection point for the axons of its
ganglion cells is the optic disc.The disc is a circular to slightly oval
structure (1.5mm), which contains a depression in the centre,the
physiological cup. The centre of the optic disc is about 4 mm nasal to
the fovea.The optic nerve head receives about 1.2 million retinal
axons ,which turn at about right angle to enter the optic nerve. Its centre
is 1.86 mm and horizontal diameter is 1.75 mm (Straatsma, Foos, Spencer, 1969) and it lies 27 mm from the nasal and 31 mm from the temporal limbus. The axons pass through the multi lamellar
fenestrations of the collagenous lamina cribrosa which occupies the
posterior scleral foramen.Optic disc head is supplied by branches of
short ciliary arteries, except for its layer of nerve fibres which is
supplied by the central retinal artery.
THE AREA CENTRALIS
The central retina is divisible into fovea and foveola, with a
parafoveal and perifoveal ring around the fovea.This region of the retina
located in the posterior fundus temporal to the optic disc is demarcated
approximately by the upper and the lower arcuate and temporal retinal
vessels and has an elliptical shape horizontally. With an average
diameter of about 5.5 mm the area centralis corresponds to
approximately 15 degree of the visual field.
FOVEA
Located at posterior pole of the globe, 4mm temporal to the centre of the
Diameter 1.85 mm , thickness o.25mm.The downwad sloping
border which meets the floor of the foveal pit is known as clivus.
FOVEOLA
It is 0.35mm in diameter and 0.13mm in thickness. Represents the area
of highest visual acuity.
MACULA LUTEA
It is an oval zone of yellow colouration within the central retina.
Yellow coloration probably derives from the prescence of carotenoid
pigment, xanthophyll in the ganglion and the bipolar cells. (Tripathi & Tripathi 1984).Pigment epithelium in the posterior fundus is less granular than at the periphery. Concentration of cone is maximum in the
central retina.Ganglion cell layer is seen in two layers at the temporal
side of the optic disc and is about 6-8 layers at the edge of the
foveola.At the foveola and optic nerve head,the ganglion cell layer is
absent.
The peripheral fundus is defined as the area anterior to the scleral
entrance of the vortex to the middle of pars plana.It is divided into
four regions – near periphery, mid periphery, far periphery and
the ora serrata.
NEAR PERIPHERY – circumscribed region of 1.5 mm around the area centralis.
MID PERIPHERY – 3 mm around the zone of near periphery.
FAR PERIPHERY – Extends 9 – 10 mm on the temporal side and 16 mm on the nasal side on the horizontal meridian.
The peripheral edge of the retina is the ora serrata.It marks the
junction between the multilayered parsplana retina and the monolayered
non-pigmented epithelium of the ciliary body.
VITREOUS BASE
Vitreous base is approximately 3.2 mm wide slightly wider
naslly and narrow temporally.Anterior portion of the vitreous base is the
zone between ora serrata and the origin of the anterior hyaloid
membrane.Anterior vitreous base is generally conformed to the contour
of the ora serrata.The posterior portion of the vitreous base is the zone
of strong retinovitreal attachment that extends posterior to the ora
AVERAGE MEASUREMENTS OF NORMAL EYE
MILLIMETERS DISC DIAMETERS
Circumference 76.85 51.0
Width of pars plana 3.80 2.5
MEASUREMENTS FROM LIMBUS TO :
Middle of pars plana ciliaris 6.10 4.0
Ora serrata 8.00 5.0
Limit between oral region and
equatorial region
Equator 13.66 9.0
MEASUREMENT IN FUNDUS:
Equator and scleral entrance 3.00 2.0
of vortex veins
Equator to ora serrata 5.66 4.0
Width of equatorial region 5.83 4.0
Width of oral region 4.73 3.0
Width of peripheral fundus 10.56 7.0
Macula to limit of 16.21 11.0
EPIDEMIOLOGY
PREVALENCE OF MYOPIA
Prevalance of myopia varies with age, sex and other factors.Most infants reach emmetropia by 2 -3 years of age. Prevalance of myopia
increase in school age and young adults reaching 20% – 25 % in mid to
latte teenage population and 25% – 35 % in young adults.Studies have
found a slightly higher prevalence of myopia in females than in
males.The prevalence of myopia increases with income level and
educational attainment and it is higher among persons who work in
occupation requiring great deal of near work.
Among children in India, Shulka found myopia to increases from
below 5% at 5 years to 20% at 20 years. Mc laren compared 2 groups of
showed better general development, also had a slightly higher
prevalence of myopia .
In an older population, Banerjee found35% of a college student
group in Calcutta to be myopic. In India, Blan observed that 42% of
people above the age group of 25 years exhibited either myopia or
myopic astigmatism.In Goldschmidt’s study the prevalence of myopia
among girls was significantly greater than that among boys. According
to APEDS study an estimated 30 million population would have
myopia,15.2 million would have hyperopia in population of more than
15 years of age.
OPTICS OF THE EYE
Emmetropia is the condition in which the parallel beam of light come to focus on the retina , with the eye at rest.At birth the average
few years of life to reach an axial length of 23mm by the age(Parsons’ Disease of eye)
Ametropia : The condition in which the incident parallel rays of light do not come to a focus upon the light sensitive layer of retina.
TYPES OF AMETROPIA
Axial ametropia : Abnormal increase in length of eyeball ( an 1mm elongation produces approx 3D of myopia).
Curvature ametropia : Abnormal curvature of the refracting surfaces of the Cornea or lens ( 1mm change in the radius of curvature
of the cornea produces a 6.00 D refractive error.
Index ametropia : Abnormal refractive indices of the media.
MYOPIA
Myopia is that form of refractive error wherein parallel rays of
light come to a focus in front of the sentinent layer of the retina when
the eye is at rest.
CLASSIFICATION OF MYOPIA Etiological Classification :
Axial Myopia :
This is the commonest type seen.It is due to an increase in the
anteroposterior diameter of the eye. For every 1mm increase will
cause 3.00 D increase in myopia.
Curvature Myopia :
This is seen due to an increase in the curvature of cornea or the surface
of the lens.
Occurs due to change in the refractive index of the media.
example - myopia seen associated with cataract and diabetes.
CLINICAL CLASSIFICATION :
Clinically there are two types of myopia.They are simple myopias
and pathological myopias.
Simple myopia :
It is the physiological variant of the normal. This is a condition of
limited progression. Simple myopia are of two types.
Physiologic Myopia :
Here each component of refraction lies upon its normal distribution
curve. Postnatal development is normal. There is correlation
failure between the total refractive power and a normal axial
diameter. The heredity is multifactorial. Myopia of -3.0 dioptres
and less is physiologic.
Intermediate Myopia :
Here there is increased expansion of posterior segment of globe.
The entire posterior segment is involved. Generalized spreading and
associated with various fundus changes can be considered intermediate
(B.J.Curtin).
Pathological Myopia :
Also called as malignant myopia. Determined by hereditary and
postnatal factors. There is excessive axial elongation of the eye
and a number of ocular complications. Myopia of -6.0 dioptres or
more is considered pathologic.
PATHOGENESIS
Pathologic myopia is characterized by degenerative changes occurring
particularly in the posterior segment of a highly myopic eye, often
associated with lengthening of the anteroposterior axis of the
globe. It connotes an extreme axial elongation in which
degenerative as well as vascular alterations are superimposed.
The most common form of pathologic myopia is the isolated
developmental form, where as in simple myopia the myopic
tendency is restrained after puberty.In developmental pathologic
myopia , the near sightedness may increase even more rapidly
during adolescence and the axial enlargement may even slowly
increase during adulthood into the 40s and 50s , with the eventual
genesis of atrophic and degenerative intraocular changes leading
Congenital axial pathologic myopia may also occur. This frequently is
associated with other congenital defects such as colobomas and
anomalies of pigmentation of the retina or choroid. The most
common associated fundus conditions resemble partial albinism.
Varying degrees of myopia commonly are associated with ROP,
microophthalmia, microcornea. microphakia, buphthalmos, the
tapetoretinal dystrophies and down syndrome.
INHERITENCE
The pathogenesis of pathological myopia remains unclear.
Previous reports have identified a locus for autosomal dominant
pathologic myopia to gene 18p11.31. More recent findings posit the
genetic heterogeneity of myopia by establishing linkage to a second
locus at the 12q2123 regions High myopia is slightly more likely to
develop in women than men, whereas the lower degrees of myopia
generally are transmitted as a dominant trait . In higher degrees of
myopia , which often begin at a relatively early age , recessive
myopia in each eye , is the rule in most cases of high pathologic myopia,
but gross inequalities greater than 3D are relatively unusual.
OCULAR CHANGES IN PATHOLOGICAL MYOPIA:
Clinically, a severe myopic eye generally appears large and prominent.
The gross appearance of the highly myopic eye is egg or pear
shaped and significantly enlarged. The cornea may be abnormally
flat , the anterior chamber is somewhat deeper than normal and
the ciliary muscles are atrophic . The ciliary muscle in a person
with high myopia often is smaller than normal , probably because
the myopic individual requires the less use of the muscles of
accommodation.
CHANGES IN POSTERIOR SEGMENT :
The major changes are confined almost entirely to the posterior
The first to correlate the histologic changes in myopia with the
ophthalmoscopic changes was Von Graefe .These changes are
summarized as follows:
1.Scleral changes – posterior enlargement of the globe and thinning of the sclera at the posterior pole with scleral ectasia and posterior
staphyloma.
2.Changes in the epipapillary and the peripapillary region - oblique entrance of the optic nerve, tilted disc , myopic crescent , nasal
supertraction.
3.Changes in the choroid and retina – atrophy and thinning , particularly affecting the posterior pole and the periphery. These
changes include atrophy and/or proliferation of the pigment epithelium,
formation of the Foster Fuchs spot at the macula, retinal microcystoid
degeneration, and occasional peripheral retinal break formation and
subsequent detachment.
4. Degenerative changes in the vitreous.
1. SCLERAL CHANGES
Scleral thinning with occasional formation of a posterior bulging or staphyloma of the sclera is common.The staphyloma may surround
the optic nerve head and extend temporally to involve the posterior pole
thickens from the equator backward, becoming thickest at the posterior
pole. In a globe with severe myopia the opposite situation occurs; the
sclera becomes progressively thinner posteriorly in the peripapillary
region. When present, a staphyloma is lined by a thin, atrophic choroids,
and the margins of the staphyloma usually reveal a relatively abrupt
edge.
TYPES OF POSTERIOR STAPHYLOMA :
Mainly five primary varieties are seen. Their features are as follows
Type I:
Here tessellation and pallor will extend over a horizontal elliptical area.
Site is nasal to disc margin commonest type seen.
Type II :
Called as macular staphyloma. Extends from the optic nerve to the
temporal aspect of macula.
Type III :
Least common type. Involves a well circumscribed area around the disc
called as peripapillary staphyloma.
Type IV :Nasal or inferonasal aspect of the optic nerve head is involved. There is associated inversion of the retinal vessels. Hence
also called as inverse myopia
Usually shallow and involves an elliptical zone below disc. Commonly
considered as a form of choroidal coloboma.
2. CHANGES IN THE EPIPAPILLARY AND PERIPAPILLARY REGIONS
Ophthalmoscopically, the optic nerve head in acquired myopia is
ovoid with the long axis in the vertical direction.Myopic degeneration
usually makes their initial appearance in the crescent margin.In severe
cases entire peripapillary area can be involved. In the typical myopic
eye the disc appears tilted with the temporal side flattened which is
surrounded by a concentric or crescent shaped area or areas of relative
fundus depigmentation.
The myopic crescent invariably occurs in later years in patients
with myopia greater than 6 D. The sclera is visible because of an
absence of pigment epithelium and choroid, both of which fail to extend
to the temporal margin of the disc. The crescent of acquired myopia are
located temporally in approximately 80% of cases. In 10% of cases, the
crescent may extend to become annular, surrounding the entire disc,
sometimes even spreading to include a large area of the fundus with
envelopment of the macular area. In rare instances, the myopic crescent
is situated on the nasal side of the disc (inverse crescent).
Atrophy of the choroids occurring predominantly near the
posterior pole is almost consistent feature of severe pathological
myopia.Initially the retinal pigment epithelium becomes attenuated and
the choroids vessels become visible.Splits may develop in Bruch’s
membrane. These form clefts (lacquer cracks or lightning
figures[German Lacksprunge and Blitzfiguren]),which seem to branch
and have a reticular appearance. During the course of pathological
myopia choroidal haemorrhages are seen. Usually seen in the macula.
Can be isolated or along with lacquer crack formation. The plane is
between retinal pigment epithelium and lamina vitrea.
LACQUER CRACKS
The ruptures of the lamina vitrea is seen as lacquer cracks. This appears as yellow white lines across posterior pole. Irregular in
caliber. Usually multiple and are horizontally oriented. They may also
show criss cross pattern. These lesions are traversed by large choroidal
vessels posteriorly. The inner layers of the retina is normal. Associated
with concentric contraction of the field. Acquired yellow blue colour
vision deficiency is also seen. If they are in macula, central vision is
impaired. Along these lesions focal areas of chorioretinal atrophy are
FORSTER FUCH’S SPOTS :
Through the defect in lamina vitrea proliferation of choroidal
fibrovascular tissues occurs. Thus a firm adhesions is seen between
choroid and retina. This fibrovascular tissue can cause haemorrhage.
There is marked proliferation of overlying retinal pigment epithelium.
This forms an unique well defined, elevated, black lesion at the posterior
pole of eye Foster Fuchs Spot.
DEGENERATIVE CHANGES IN THE VITREOUS :
Vitreous changes including liquefaction, microfibrillar degeneration and
formation of opacities and floaters (muscae volitantes) may occur.
Posterior detachment of the vitreous commonly occurs, probably
because of stretching of the enlarged globe, leaving a gap
between the posterior vitreous and the posterior pole of the eye.
DEGENERATIONS OF THE PERIPHERAL RETINA Retinal hole
Is a more advanced tropic lesion, is manifest grossly as a round
complete retinal break without detectable flap or operculum.
These holes are commonly found in the anterior zone, usually in
Cystoid degeneration
Inner wall of single cyst may be absent or broken giving the
appearance of retinal hole. This is a pseudo-hole since the outer wall of
the cyst is intact.
Another type of cystoid degeneration is the reticular cystoid
degeneration of the peripheral retina, is almost invariably located
posterior to and continuous with the typical cystoid degeneration.
Retinal cystoid degeneration is present in 18% of adult patients, most
prevalent in the infero – temporal quadrant.
Retinoschisis
This condition is a splitting of the neural layers of the retina
which generally occurs in the outer plexiform layer. Typical
degenerative retino schisis is a more extensive tropic process and
presents as a round or oval area of retinal splitting with a smooth
fusiform elevation of the inner layer and its blood vessels.
Paving stone degeneration:
Is characterized by one or more discrete rounded foci of depigmentation and retinal thinning located between the ora serrata and
underlying choroidal vessels and often has a pigmented margin. The
basic lesion is rounded in shape and is one to several disc diameters in
size , clusters of hese rounded foci may merge to form larger lesions
with scalloped margin and incomplete pigmented septum.
Histologically characterisied by loss of retinal pigment epithelium
and the outer retina with adhesion of the inner retina to the Bruch’s
membrane.
Paving stone degeneration does not predispose to retinal break or
retinal detachment.
Chorioretinal degeneration:
This condition always extends round the fundus periphery. It
begins and is most severe in the retina adjacent to the ora serrata. It
spreads posteriorly and merges into the normal healthy retina without
definite demarcation. Chorio-retinal degeneration is frequently
associated with cystoid degeneration, both conditions more or less
occupying the same area.The ophthalmoscopic appearance of
chorio-retinal degeneration can be graded as mild, moderate or severe.
The changes are always severe adjacent to the ora serrata and
mildest further posteriorly. Peripheral chorio-retinal degeneration begins
to appear in the fourth decade of life and increase severely with the age.
Chorio- retinal atrophy:
Is characterized by discrete areas of retinal and choroidal thinning. Pigment proliferation, and migration of the pigment in the
retina re present around the edges of the lesion whose centre is pale and
dirty grey. Atrophy of the inner choroidal layer clearly expose the large
choroidal vessels.
Pigmentary degeneration:
Of the various types of peripheral changes, pigmentary
degeneration is the leasts studied and least understood lesion. The
pigmentation may vary from a fine diffuse darkening of the fundus to
the presence of large discrete clumps. Pigment may be found in
scattered clumps or granules or as localized clumps or may be diffusely
distributed.Pigmentary degeneration has a tendency towards bilaterality
and apparently no sex preference. Age does not seem to be an important
factor.It has a tendency to be found with white without pressure or
lattice degeneration or associated with silent retinal breaks.
White without Pressure :
Circumferentially arranged geographic white or grey areas are
quadrant, posterior to the equator. The surface is covered by glistening
yellow white dots and fine lines.
White with Pressure :
Usually found in area of lattice and small retinal breaks. Also seen
in eyes with vitreous and retinal detachments. These degenerative
changes are benign lesions.
Lattice Degeneration :
Most common lesion linear or spindle shaped lesions are seen at or
peripheral to equator. Sharply demarcated and circumferentially
oriented. Variable amount of pigment proliferation is also seen. At the
margins of these lesions vitreous adhesions are seen. Also associated
with round holes. If traction present then tears are formed which cause
detachment.
Opthalmoscopically over these lesions white interlacing lines are
seen. They are hyalinized blood vessels which forma criss cross pattern.
These lesions enlarge circumferentially and new lesions also form.
Bilaterally involves superior temporal quadrant. Flourescein
angiography shows poor or absent perfusion in these areas
COMPLICATIONS
4. severe visual impairment. 5. chronic simple glaucoma.
CLINICAL EVALUATION FOR
PATHOLOGICAL MYOPIA
1. Visual acuity – Is the most important criterion of testing the
functional integrity of the eye.
2. Direct ophthalmoscopy – Though the area of field observed is
smaller, increased magnification obtained with this method allows
detailed examination of the various details of the fundus.
3. Indirect ophthalmoscope – This technique is of special importance because it allows the examiner to form a clearer
understanding of the cause and forces involved in the various
pathological features involving retina and all the features are
documented in a retina chart.
4. Fundus fluorescein angiography – Used to detect posterior pole
changes like SRNVM,foster fuch’s spots, lacquer cracks and early
macular hole in cases of pathological myopia.
5. Indocyanine green angiography – Is superior to FFA in studying choroidal lesions because of certain physical properties of ICGA
dye.Choroidal circulation and areas of neovascularisation lying
beneath the retina show much better with ICGA.
neovascularisationof the choroid and leakage of the disc.Also
seen in areas of atrophy of pigment epithelium.
6. Ascan – Is a one dimensional display in which echoes are represented as vertical spikes from a baseline.Ascan biometry
helps to differentiate axial myopia from lenticular myopia.A
posterior staphyloma in highly myopic eyes causes an increase in
axial length.
7 Bscan – Produces a two dimensional acoustic section, hence echo
is represented as a dot on the screen rather than a spike.In high
myopic eyes it can be used to evaluate the posterior segment
which can have retinal detachment, retinal tears. Posterior
staphyloma is seen as a shallow excavation of the posterior pole
with smooth edges on sonographic evaluation of highly myopic
eyes.
8 Optical coherence tomography – A new diagnostic technology
which provides a cross sectional image of the retina in vivo with a
high resolution similar to histological section by a light
microscopy. OCT can be used to diagnose a foveal retinal
detachment with retinoschisis which are common features in
MANAGEMENT
Treatment of pathologic myopia may be divided into 3 goals –
visual rehabilitation of the patient, prevention of myopic progression
and the management of a variety of complicating diseases.
Visual rehabilitation Optical :
Spectacles – patients should be advised about the type of frame and the material of the lenses which are suitable for those patients with high
myopia. High-index glass, plastic and polycarbonate lenses are suitable
for high myopic patients.Special edge polishing and buffing can also
improve lens cosmetics.
Contact lenses – contact lenses are of special value in high myopia because they afford a dramatically improved appearance and
enhance the visual acuity by reducing the image minification and
expand the visual field. Both soft and gas-permeable contact lens
designs are plausible.In cases of high myopia, it may be necessary to
specify a minus-edge lenticular design to minimize the complications
and discomfort of a thickened skirt.
Surgical :
Surgical correction of high myopia can be attempted through ,
1. The flattening of corneal curvature for lower degrees.
2. Insertion of IOL into the phakic anterior chamber.
3. The removal of clear crystalline lens.
4. Shortening of axial diameter by scleral resection.
5. Role of LASIK in high myopia is controversial.
Low vision aids – in cases of high myopia, the most useful low vision aid for distance is use of telescopic lens. New models with a
small telescopic lens fitted into patients spectacles may be of great use.
Ocular hygiene :
Ocular hygiene has undoubtedly greatly emphasized as an adjunct
to the control of myopic progression.
MANAGEMENT OF COMPLICATIONS
1. Retinal breaks and detachment
Treatment of retinal breaks is much rewarding than is, the
attempted repair of an advanced detachment. Yanoff has recommended
then carrying out the treatment of ora.Retinal detachment surgery should
be done taking into consideration of factors of scleral thinning and
posterior staphyloma.
1. Choroidal neovascular membrane
a) Extra foveal CNVM – Green 514nm / Red 647 nm laser
( ≥200µm from to cover CNVM.
centre of FAZ )
b) Juxta foveal CNVM – Laser to cover CNV contigous
(<200µm & ≥ 1µm blockage and 100 m beyond on
from centre of FAZ) non foveal side
c) Sub foveal – Photodyanamic therapy
2. Ocular hypertension and glaucoma management
The goal of glaucoma treatment is to preserve good visual
function for the patients life time.This can be attained by lowering the
intraocular pressure to a level that will stop or atleast slow the
progression of optic nerve damage and its consequent vision loss.
3. Management of cataract
Either phacoemulsification or SICS with proper IOL implantation
has to be done taking proper precautions to prevent complications.
4. Management of strabismus and amblyopia
Early squint correction is accepted as the most beneficial
approach to congenital tropias associated with myopia(Taylor).
Appropriate spectacles and occlusion therapy is advocated to manage
amblyopia.
5. Management of retinitis pigmentosa
Low vision aids and genetic counselling.
6. Newer modality of treatment - intravitreal injection of Bivacizumab seems to be an effective and safer treatment for macular
Aim of the Study
AIM OF THE STUDY
1. To analyze the clinical features and biometric parameters in
pathological myopia.
2. To analyze the visual parameters in relation to posterior polar
changes and disc changes.
3. To study the incidence of retinal degenerations and detachment in
pathological myopes.
4. To analyze the association of other ocular association like lens
changes, open angle glaucoma, retinitis pigmentosa, strabismus in
cases of pathological myopia.
Materials and
methods
This study was carried out at Retina clinic, Regional Institute of
ophthalmology and Government ophthalmic hospital Chennai from
December 2004 to September 2006 . This is a prospective study.Cases
were registered, evaluated, treated and followed up during the study
period.
Inclusion criteria :
a. Patients with a refractive error of > 6.00 D.
b. Patients with normal corneal curvature.
c. Patients with axial length of > 24 mm.
Exclusion criteria :
a. Patients with index myopia.
b. Patients with abnormal corneal curvature.( curvature myopia were
excluded).
c. Low degrees of myopia and congenital myopia.
d. Other ocular pathologies like micro ophthalmos, ROP, ectopia
lentis were excluded.
Myopic patients attending the RIO GOH - OPD between the
period December 2004 to September 2006 were selected
randomly – criteria applied.
1. History of refractive error including
- duration
- age at which spectacle were worn for the first time
- time of last change of spectacles
- complaints with present spectacles.
- Family history of myopia.
2. History of other symptoms like progressive loss of vision,
defective vision related to day or night, sudden loss of vision, flashes
and floaters.
All of them were subjected to routine ophthal examination
including refraction and detailed fundus examination with drawing and
were documented.
Anterior segment SLE was done to rule out other pathology. Routinely
IOP was measured by applanation tonometer for all the patients. The
axial length was measured using Ascan biometry and keratometer was
done. Those with abnormal K- reading were excluded from the
Those patients with posterior pole changes were picked up for
further investigations. Patients with macular pathology were followed
up with FFA and documented. Those with posterior staphyloma were
confirmed with B scan. The incidence of various degenerations were
recorded and analyzed , evaluated and treated accordingly. Those
patients who presented with complications as well as who had
complications during the study period were treated accordingly. Those
with retinal tears were treated with barrage LASER and also with
Observation &
Analysis
OBSERVATION & ANALYSIS
Incidence of pathological myopia was common in the age group
of 21 to 30 years,i.e in young adults which correlated well with
Framingham Eye study group.
2) ANALYSIS DEPENDING ON SEX
Sex appears to have an influence on incidence. Females are prone
to higher degrees and to degenerative changes of pathological myopia
myopia. (Arun verma et al)
Age in Number of patients
Percentage
0 -10 3 6%
11-20 15 30%
21-30 19 38%
31-40 7 14%
41-50 4 8%
>50 2 4%
Sex of patient No of patients Total %
Female 27 54%
3) ANALYSIS DEPENDING ON OCCUPATION
Occupation Number of patients
Percentage
Student 26 52%
House wife 8 16%
Engineer 5 10%
Teacher 2 4%
Clerk 3 6%
Labourer 3 6%
Others 3 6%
Majority of patients in this study were from student community.
4) ANALYSIS DEPENDING ON FAMILY HISTORY
Out of 50 cases examined only 9 cases (18%) had positive family
history, and this can be attributed to lack of awareness mainly in low
socioeconomic group.
5) ANALYSIS DEPENDING ON EYES INVOLVED
Total No of cases 50
No of cases with family history 9
Out of 50 cases of pathological myopia 46 had bilateral presentation
and only 4 persons had unilateral occurrence.
6) ANALYSIS DEPENDING ON UNCORRECTED VISUAL ACUITY Eyes involved Total Percentage Unilater al
4 8%
Bilatera l
46 92%
Visual acuity Number of eyes involved
Percentage
6/60 – 4/60 33 34.37%
4/60 – 2/60 35 36.45%
2/60 – 1/2/60 17 17.70%
Out of 96 eyes studied majority of patients had an uncorrected
visual acuity ranging from 4/60 to 2/60 which was closely followed by
6/60 to 4/60 group.
7) ANALYSIS DEPENDING ON REFRACTIVE STATUS
Refractive status Number of eyes Percentage
-6 to -10 D 35 36.45%
-10 to -14 D 31 32.29%
-14 to -18 D 7 7.29%
-18 to -22 D 7 7.29%
> - 22 D 3 3.12%
Among 50 patients nearly 80 % of study group had refractive
error ranging from -6.0 D to – 14.0 D .
8) ANALYSIS DEPENDING ON BEST CORRECTEDVISUAL ACUITY
BCVA Number of eyes Percentage
6/6 – 6/18 18 18.75%
6/18 – 6/36 35 35.41%
6/36 – 6/60 23 23.95%
6/60 – 1/60 7 7.29%
About 35% of the patients had a best corrected visual acuity of
6/18 to 6/36, after proper retinoscopy and refraction. Vision correction
in high myopic eyes is obviously decreased with increase in dioptres.
9.ANALYSIS DEPENDING ON AXIAL LENGTH
Majority of eyes included in the study had an axial length ranging
between 26 mm to 28 mm.( Lin L.L, Shih. Y.F,Lee.Y.L). Axial elongation of the eyeball is the main component in myopic progression.
10) ANALYSIS DEPENDING ON INTRAOCULAR PRESSURE Axial length
(in mm)
Number of eyes
Percentage
24 – 26 7 7.29
26 – 28 59 61.45
28 – 30 22 22.91
Out of 96 eyes in the study group, about 4% had an ↑ed IOP of more
than 20mm of Hg by applanation tonometry.Nearly 80% patients
in this study had a normal IOP.
11) ANALYSIS OF VITREOUS PATHOLOGY
IOP Number of eyes Percentage
< 10 4 4%
10 – 12 5 5%
12 – 14 30 30%
14 – 16 30 30%
16 – 18 21 21%
18 – 20 6 6%
About 20% of pathological myopia presented with vitreous
strands and fibrillation and 14% with PVD indicating more than 50%
had vitreous pathology at the time of presentation itself (Morit H et al ).
12) ANALYSIS DEPENDING ON VARIOUS RETINAL CHANGES IN THE POSTERIOR POLE
Retinal changes Number of eyes Percentage
Posterior staphyloma 10 10.41%
Temporal crescent 44 45.83%
Tigroid fundus 47 48.94%
Peripapillary atrophy 33 34.37%
CRAP 28 29.16%
Vitreous pathology Number of eyes. Percentage
Vitreous fibrillations and strands
22 22.91%
SRNVM 5 5.20%
Lacquer cracks 2 2.08%
Forster fuchs spots 4 4.16%
Bony spicules 10 10.41%
Medullated nerve fibre 1 1.04%
Retinoschisis 1 1.04%
Macular Pigmentary stippling 3 3.12%
Majority of the patients in this study group had temporal
crescent and tigroid fundus as a common feature.10% of the patients had
posterior staphyloma. Lacquer cracks were seen in 2% of the patients
.Forster fuchs spots were seen in 4% of the patients. Chorio retinal
atrophic patches were seen in 29% of the patients which correlated well
with the study conducted by Brasil et al. SRNVM was seen in 4% of
the patients which is in concordance with the study conducted by
Ohno-Matsui K
13) ANALYSIS OF RETINAL CHANGES IN PERIPHERY
Retinal changes Number of eyes Percentage
Lattice degeneration 13 13.54%
Paving stone degeneration 10 10.41%
WWOP 9 9.37%
Snail track degeneration 5 5.20%
Lattice degeneration was the commonest type of peripheral
degeneration noted in the study , followed by paving stone degeneration,
which coincides well with the study by Celorio , Preutt R C.
14) ANALYSIS OF OTHER OCULAR FINDINGS Condition Number of eyes Percentage
RP 10 10.41%
Retinal detachment 9 9.37%
Postr subcapsular cataract
8 8.33%
SRNVM 5 5.20%
POAG 4 4.16%
Strabismus 2 2.08%
Retinoschisis 1 1.04%
Higher incidence of Pigmentary dystrophy (10.4%) was noted in
the study group, followed by RD (9.37%).Other associations noted were
Posterior sub capsular cataract. (Beaver Dam eye study), increased intra
ocular pressure ( Blue mountain study) and strabismus(2%)..
15) CONDITIONS PREDISPOSING TO RETINAL DETACHMENT
Peripheral degenerations
Number of eyes Percentage
Lattice degeneration 11 11.45%
Snail track degeneration 6 6.25%
White without pressure 9 9.37%
Lattice degeneration with hole was commonest among the
predisposing factors for retinal detachment, followed by white without
pressure.
16) ANALYSIS DEPENDING ON CONDITIONS NOT PREDISPOSING TO RETINAL DETACHMENT
Condition Number of eyes
Paving stone degeneration 11
Percentage 11.45%
Paving stone degeneration was the 2nd common degeneration
noted in the study.
17) ANALYSIS DEPENDING ON K READING
K Reading Number of patients Percentage
44 – 45 29 30.20%
45 – 46 25 26.04%
46 – 47 32 33.34%
The corneal curvature in this group was in the normal range as
those with a higher curvatures were excluded.
18) ANALYSIS DEPENDING ON LATTICE DEGENERATION IN DIFFERENT QUADRANTS .
Quadrant Number of eyes Percentage
Supero Temporal 7 63.30%
Supero Nasal 1 9.09%
Infero Temporal 1 9.09%
Infero Nasal 2 18.18%
Lattice degeneration was most commonly located in the supero –
temporal quadrant (63.3%).
19) ANALYSIS OF INCIDENCE OF RETINAL DETACHMENT IN DIFFERENT MYOPIC STATUS
Diopteric power
( in spheres) Number of patients Percentage
<10 D 3 30%
Among the RD cases, patients with less than 10 dioptres had 30%
incidence of RD, where as those with more than 10 dioptres had 70 %
incidence of RD.This indicates that the risk for RD increases with the
Discussion
• 96 eyes of 50 patients with pathological myopia were studied, of which its incidence was common between the age group 21 to 30
years , which correlated well with Framingham Eye study group ,
suggesting that aging in addition to mechanical stretching is also
important for the development of the fundus changes.
• Sex appears to have an influence on incidence. Females are more
prone to higher degrees of myopia as well as degenerative
changes occurring in high myopia.
• Only 8%of cases had family history of myopia , majority of the
cases did not have a significant family history. Reduced incidence
may be due to lack of awareness among the low socio economic
group.
• Majority of patients in this study were from student community
which suggests that those people are more aware of their
refractive error and seek ophthalmic opinion earlier.
• Out of 50 cases of pathological myopia 46 had bilateral presentation and only 4 persons had unilateral occurrence. In
acuity as well as binocular vision is expected if timely and
consistent therapy is administered.
• Nearly 80% of patients with myopia fell into the dioptric range of
- 6 to -14 D, which indicates that extreme degrees of myopia is
relatively less frequent and suggests that greater the dioptre is,
harder the vision can be ideally corrected.
• Majority of eyes included in this study has an axial length ranging
between 26 – 28mm (Liull et al), which shows that axial elongation of the eye ball is the main component causing myopic
progression.
• Among the study group, about 4%had an elevated IOP of more
than 20 mm Hg by applanation tonometry (Blue mountain study
group).
• Out of 96 eyes even after full correction with glasses, in majority
of them (36%) BCVA improved to only 6/18 to 6/36, which
can be ideally corrected.The greater the pathologic changes at the
posterior pole , the severer the degree of damage(Journal Eye
Science: 2003 Dec 19(4) 211 – 4 )
• More than 50% of cases in this group had vitreous abnormalities
which suggests that liquefaction of the vitreous begins at an
earlier age in patients with high myopia and progresses with age
and axial elongation and thus results in a frequent occurrence of
PVD(14%)-Morita h,Funata M et al Retina 1995 15(2):117-24.
• Majority of patients in this study group had temporal crescent and
tesselated fundus as a common feature followed by Posterior
staphyloma- 10%,SRNVM – 5.20%, Forster Fuchs spots – 4.16%
and Lacquercracks–2.08%, which correlates well with the study
conducted by Brasil et al (Arq.Bras Ophthal Mar-April,69(2)
203-6).
• Lattice degeneration was the commonest type of peripheral
degeneration is influenced by the amount of axial elongation in
highly myopic eyes.(Amj : 1991 Jan 15 (11) 1:20:3).
• a) Myopic patients had higher risk of glaucoma compared with
that of non myopic subjects(Ophthalmology 2000 Jun 107(6)
1026-7 -The blue mountain study).
b) Other associations noted were Posterior subcapsular cataract
(Lim et all) ,Strabismus , Retinitis pigmentosa and Retinal detachment.
• Among the predisposing factors leading to RD, lattice with hole
was the leading factor followed by paving stone degeneration.
Among the number of lattice degeneration noted majority of them
were seen in the supero temporal quadrant probably due to
excessive stretching and increased vascularity in this area.
• Patients with refractive status of more than 10 D showed a higher
risk of RD , showing that the risk of RD is directly proportional to
the higher degrees of myopia (ie, axial lengthening).
posterior pole. This information may be useful when evaluating
and following patients with moderate to high degrees of myopia
Summary
• 96 eyes of 50 patients with pathological myopia were analysed based on their axial length, corneal curvature and ocular fundal
changes at the posterior pole and in the peripheral retina
• Highest incidence of pathological myopia was noted in the age
group between 21 – 30 yrs
• The majority of patients did not have significant family history. 8% had unilateral myopia on presentation.
• Majority of patients in my study were found to be students
which says that the most common environmental factor could
be increasing education & higher amounts of near work.
• About 70% of the patients had an UCVA ranging between
2/60-6/60.
• 80% of the patients with pathological myopia fell into the dioptric range between – 6 to -14 dioptres. Very high degrees
• High degree of myopia had a definite correlation with increase in axial length.
• The higher the refractive power the more difficult is to achieve a near normal vision, which establishes the fact that
pathological changes in the posterior pole is responsible for
the defective vision.
• More than 50% of the cases showed vitreous abnormalities
showing the early onset of vitreous degeneration in high
myopes.
• Lattice degeneration was the commonest type of peripheral degeneration noted and was seen mostly in the super temporal
quadrant.
• Majority of the patients had temporal crescent and tessellated
fundus as a common feature.
• About 2% of eyes showed lacquer cracks and Forster Fuchs spots was seen in 4.16% of eyes.
• Choroidal neovascularisation was seen in 5% eyes.
• Retinitis pigmentosa, retinal detachment, glaucoma, posterior
subcapsular cataract were the common ocular associations
seen in high myopic patients.
• Hence this study brings forth the various factors that may be
useful while evaluating & following up of patients with
moderate to high degrees of myopia.
Conclusion
CONCLUSION
Pathological myopia is a complex eye disease in which the
patients not only present with visual morbidity but also have a diseased
eye. Hence they have to be approached according to their needs &
Degenerative changes are more commonly seen in higher degrees
of myopia & so all cases of myopia must be examined meticulously
with indirect ophthalmoscope which can pick up complications at the
earliest & can be treated effectively. This can aid in retaining useful
ocular function. Awareness need to be created among myopic
population regarding visual hygiene, safety precautions, risks &
complications involved.
They have to be informed about the warning signs & symptoms
to report early for better management. hence all patients with
pathological myopia should be monitored periodically.
Proforma
PROFORMA
1 . Case N o : Hospital No :
2. Name :
3. Age : Sex :
4. History :
Defective vision : Day / Night
Floaters :
Wearing spectacles since :
Last change of spectacles : Family H/O myopia :
5. General Examination :
6. Systemic Examination :
7. Local Examination :
RE LE
Vision :
I.O.P :
Retinoscopy :
Best corrected visual acuity :
Anterior Segment :
A-Scan/ Keratometry :
Fundus (Direct Ophthalmoscopy)
Disc/Cup :
Colour :
Size :
Cup :
Crescent :
Blood Vessels :
Macula :
Back Ground :
Indirect Ophthalmoscopy :
3 mirror contact lenses :
8. Observations :
Type of degenerations found
a. Pigmentary
b. Paving stone
c. Lattice
d. Chorio - retinal
e. White without pressure
f. White with pressure
g. Snail track degeneration
h. Retinal break
a. Supero Temporal
b. Supero Nasal
c. Infero Nasal
d. Infero Temporal
10 . Eyes :
a. Unilateral
b. Bilateral
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KEY TO MASTER CHART
F/H - Family History
VA - Visual Acuity
Ref. Power - Refractive Power
AL - Axial length
F.Changes - Fundus changes
RE - Right Eye
LE - Left Eye
Wnl - Within normal limits
VF - Vitreous floaters
Tess - Tesselation
Temp - Temporal
LD - Lattice degeneration
STD - Snail track degeneration
PSD - Paving stone degeneration
PVD - Posterior vitreous detachment
PS - Posterior staphyloma
RT - Retinal tear
RD - Retinal detachment
WWP - White with pressure
WWOP - White without pressure
STQ - Supero temporal quadrant
SNQ - Supero nasal quadrant
INQ - Infero nasal quadrant
SQ - Superior quadrant
BG - Best glasses
EXP - Explant
Pro.Cryo - prophylactic cryotherapy
PR - Periodic review
PPC - Posterior polar cataract
ANALYSIS DEPENDING ON AGE
0 - 10 6 %
11- 2 0 3 0 %
2 1- 3 0 3 8 % 3 1- 4 0
14 %
4 1- 5 0 8 %
>5 0 4 %
0-10 11-20 21-30 31-40 41-50 >50
